Teachers of English as a foreign language in Taiwan are challenged to organize multi-dimensional language activities for foreign students coming from ASEAN countries, including Japan, the Philippines, South Korea, and Vietnam. With different cultural backgrounds, these students have different prior knowledge of Taiwanese culture, and, because of the similarities and differences between Taiwan and these countries, it is meaningful to explore the development of globalization with the students, who are learning both English and Chinese. The different historical backgrounds, various cultural and religious differences, and social conditions, such as gender relationships in working places, are significant topics for class discussions. When teachers serve as discussion facilitators, they encourage students to express their own multi-identities and expectations for the exchange program. Most interesting of all is to find out about their own short-term and long-term career goals. 32 foreign students from the Philippines and Vietnam were recruited for research. Questionnaires were used to assess their foreign language learning motivation and strategies, as well as to discover the learning environment they prefer and their globalization prospects. It was found that multi-lingual language policies for promoting globalization in higher education are very likely to influence the success of foreign student study in Taiwan.

Neuronal cell death in the central nervous system has always been a challenging process to decipher. In physiological condition, neuronal cell death is restricted in the adult brain even as people ages. However, in pathological conditions of various neurodegenerative diseases, the cell death and shrinkage of a specific brain region represent a fundamental pathological feature across different neurodegenerative diseases. In this review, we will briefly go through the general pathways of cell death and describe the evidence of the cell deaths in the context of common neurodegenerative diseases individually, discussing our current understandings of cell death in connecting with the renowned pathogenic proteins, including tau, amyloid-beta, alpha-synuclein, huntingtin, and TDP-43.

Human colon carcinomas, including HCT116 cells, often exhibit high basal autophagic flux under nutrient deprivation or hypoxic conditions. Mitochondrial ROS (mROS) is known as a “molecular switch”’ for regulating the autophagic pathway, which is critical for directing cancer cell survival or death. In early tumorigenesis, autophagy plays important roles in maintaining cellular homeostasis and contributes to tumor growth. However, the relationships between mROS and the autophagic capacities of HCT116 cells are poorly understood. Ubiquinol cytochrome c reductase binding protein (UQCRB) has been reported as a biomarker of colorectal cancer, but its role in tumor growth has not been clarified. Here, we showed that UQCRB was overexpressed in HCT116 cells compared to CCD18co cells, a normal colon fibroblast cell line. Pharmacological inhibition of UQCRB reduced mROS levels, autophagic flux, and the growth of HCT116 tumors in a xenograft mouse model. We further investigated mutant UQCRB-overexpressing cell lines to identify functional links in UQCRB-mROS-autophagy. Notably, an increasing level of mROS caused by UQCRB overexpression released Ca2+ by activation of lysosomal TRPML1 channels. This activation induced transcription factor EB nuclear translocation and lysosome biogenesis, leading to autophagy flux. Collectively, our study showed that increasing levels of mROS caused by overexpression of UQCRB in human colon carcinoma HCT116 cells could be linked to autophagy for cell survival.

Photocatalytic degradation plays a crucial role in wastewater treatment, and the key to achieving high efficiency is to develop photocatalytic systems that possess excellent light absorption, carrier separation efficiency, and surface-active sites. Among various photocatalytic systems, S-type heterojunctions have shown remarkable potential for efficient degradation. This work delves into construction of S-type heterojunctions of ternary indium metal sulfide and bismuth ferrite nanofibers with introduction of sulfur vacancy defects and morphology modifications to enhance the photocatalytic degradation performance. Through the impregnation method, BiFeO₃/Zn₂S₄ heterojunction materials were synthesized and optimized30% BiFeO₃/Zn₂S₄ heterojunction exhibited superior photocatalytic performance with higher sulfur vacancy concentration than Zn₂S₄. The in-situ XPS results demonstrate that the electrons between Zn₂S₄ and BFO are transferred via S-Scheme, and after modification, Zn₂S₄ has a more favorable surface morphology for electron transport, and its flower-like structure interacts with the nanofibers of BFO, which has a further enhancement of the reaction efficiency for degrading pollutants. This exceptional material demonstrated a remarkable 99% degradation of Evans blue within 45 min and a significant 68% degradation of ciprofloxacin within 90 min. This work provides a feasible idea for developing photocatalysts to deal with the problem of polluted water resources under practical conditions.

Manipulating autophagy is a promising strategy for treating cancer as several autophagy inhibitors shown to induce autophagic cell death. One of these, autophagonizer (APZ), induces apoptosis-independent cell death by binding an unknown target via an unknown mechanism. To identify APZ targets we used a label-free drug affinity responsive target stability (DARTS) approach with a liquid chromatography/tandem mass spectrometry (LC-MS/MS) readout. Of 35 protein interactors, we identified Hsp70 as a key target protein of unmodified APZ in autophagy. Either APZ treatment or Hsp70 inhibition attenuates integrity of lysosomes, which leads to autophagic cell death exhibiting an excellent synergism with a clinical drug, temozolomide, in vitro, in vivo, and orthotropic glioma xenograft model. These findings demonstrate the potential of APZ to induce autophagic cell death and its development to combinational chemotherapeutic agent for glioma treatment. Collectively, our study demonstrated that APZ, a new autophagy inhibitor, can be used as a potent antitumor drug candidate to get over unassailable glioma and revealed a novel function of Hsp70 in lysosomal integrity regulation of autophagy.

Neuronal cells are believed to rely on autophagy to maintain cellular homeostasis. Nevertheless, autophagy may be a therapeutic target for neurodegenerative diseases because of the role it plays in neuronal cell death. Despite Beclin 1 association with autophagy and apoptosis, the molecular mechanisms that underlie Tau-induced vesicular pathology and Tau protein aggregates in humans remain poorly understood. Here, we set out to examine the role of three genes-ATG14L, Beclin 1 and VPS34- in autophagy nucleation failure-associated Tau disorders in fruit fly models. We found that either reduced ATG14L levels improve neuronal outcomes, or transgenic expression of ATG6/Beclin 1 greatly reduced age-dependent neurodegeneration and Tau pathology; whereas, the loss of Beclin 1 exacerbated these effects. Prior to p-Tau accumulation, the neuronal Beclin 1 network is critical for reducing p-Tau accumulation, indicating that the loss of Beclin 1 causes Tau pathology and neurodegeneration. As neurodegeneration progressed, glial cells showed an upregulation of vesicular Beclin 1 immunoreactivities. The reduced VPS34 also resulted in p-Tau accumulation, suggesting that neurons require both Beclin 1 and VPS34 to reduce p-Tau accumulation. Our results provide mechanistic insight into the molecular pathways that cause age-dependent Tau pathology and neurodegeneration due to an excess of autophagy nucleation processes and autophagy activity, and we derive novel inferences on the therapeutic possibilities of rebalanced Beclin 1 network by reducing autophagic specific nucleation component of ATG14L.